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Maternal Regulation of Embryonic Growth: The Role of Vasoactive Intestinal Peptide¹

Section on Developmental and Molecular Pharmacology (C.Y.S., S.J.L., G.G., D.T.A., R.A., D.E.B., J.M.H.), Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892; and Division of Neonatology (S.K.M.), Children’s National Medical Center, Department of Pediatrics, George Washington University, Washington, D.C. 20010

Address all correspondence and requests for reprints to: J. M. Hill, Ph.D., Section on Developmental and Molecular Pharmacology, Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Building 49, 5A-38, MSC 4480, 9000 Rockville Pike, Bethesda, Maryland 20892. E-mail: jh139h{at}nih.gov

Vasoactive intestinal peptide (VIP) is an important growth regulator of the embryonic day (E)9–E11 mouse. In comparably aged rat embryos, VIP messenger RNA (mRNA) is not detectable; however, peak concentrations of VIP in maternal rat serum indicate a nonembryonic source. In the current study, mouse maternal and embryonic tissues were examined from E6–E12. Although RT-PCR revealed VIP mRNA in E6–E7 conceptuses, by E8 (when extraembryonic tissues could be separated from the embryo), VIP mRNA was detected only in the decidua/trophoblast. Decidual/trophoblastic VIP mRNA decreased until E10, after which it was not detectable. VIP mRNA was not apparent in the embryo until E11–E12. At E9, VIP immunoreactivity was localized to abundant, diffuse cells in the decidua basalis, which were also immunoreactive for T cell markers. VIP binding sites were dense in the decidua/trophoblast at E6, but gradually decreased until E10, after which they were not apparent. VIP binding sites were detected in embryonic neuroepithelium by E9. The transient presence of VIP binding sites and mRNA in the decidua/trophoblast correlate with the critical period of VIP growth regulation, when VIP mRNA is absent in the embryo. These findings suggest that maternal lymphocytes are the source of VIP’s regulating early postimplantation embryonic growth.

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